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目的探讨选择性COX-2抑制剂塞来昔布对SGC-7901人胃癌细胞钠氢交换体1(NHE1)表达及细胞内pH的影响。方法以SGC-7901人胃癌细胞为研究对象,不同浓度的塞来昔布(5、12.5、25、50、75和100μmol/L)作用于SGC-7901细胞不同时间后,采用MTT法检测塞来昔布对胃癌细胞生长的抑制作用;采用Western blot技术检测不同浓度塞来昔布对SGC-7901细胞NHE1表达的影响;在此基础上,采用BCECF-AM免疫荧光测定不同浓度塞来昔布对SGC-7901细胞内pH的影响。结果塞来昔布能抑制SGC-7901细胞的生长,在一定范围内,其抑制作用随着塞来昔布浓度的增加而增强;同一浓度条件下,其抑制作用随着作用时间的延长也相应增强(P<0.05)。不同浓度塞来昔布(除5μmol/L组外)作用于SGC-7901细胞后,NHE1表达均有下调,并呈浓度依赖性(P<0.05)。SGC-7901细胞内pH为碱性,不同浓度(除5μmol/L组外)塞来昔布干预24 h后,SGC-7901细胞内pH较对照组细胞明显下降(P<0.05),并且下降情况呈浓度依赖关系(P<0.05)。结论塞来昔布对SGC-7901细胞生长抑制作用可能通过下调NHE1表达和降低细胞内pH实现。
Objective To investigate the effect of selective COX-2 inhibitor celecoxib on the expression of sodium hydrogen exchanger 1 (NHE1) and the intracellular pH of human gastric cancer cell line SGC-7901. Methods SGC-7901 human gastric cancer cells were treated with different concentrations of celecoxib (5, 12.5, 25, 50, 75 and 100 μmol / L) on SGC-7901 cells at various times, The effect of different concentrations of celecoxib on the expression of NHE1 in SGC-7901 cells was detected by Western blot. On the basis of this, BCECF-AM immunofluorescence was used to determine the effect of different concentrations of celecoxib Effect of SGC-7901 intracellular pH. Results Celecoxib could inhibit the growth of SGC-7901 cells, and its inhibitory effect increased with the increase of celecoxib concentration within a certain range. With the same concentration, the inhibitory effect of celecoxib also increased with the prolongation of acting time Enhanced (P <0.05). After treated with different concentrations of celecoxib (except 5μmol / L), the expression of NHE1 was down-regulated in a concentration-dependent manner (P <0.05). The intracellular pH of SGC-7901 cells was alkaline, and the intracellular pH of SGC-7901 cells decreased significantly (P <0.05) compared with that of the control group after 24h intervention with different concentration of celecoxib (except 5μmol / L group) Concentration-dependent (P <0.05). Conclusion Celecoxib inhibits the growth of SGC-7901 cells by down-regulating NHE1 expression and decreasing intracellular pH.